Fetal Distress 3

7/25/2019 Fetal Distress 3

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Fetal Distress


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What is fetal distress?

Fetal distress is the term commonly used todescribe fetal hypoxia. It is a clinical diagnosis

made by indirect methods and should be definedas:-

Hypoxia that may result in fetal damage ordeath if not reversed or the fetus delivered

immediately. More commonly a fetal scalp pH of less than 7. isused to indicate distress


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Etiology

Fetal oxygen supplied from:

!maternal circulation-----placenta------umbilical

cord------fetus maternal factors

!cardiovescular diseases

!acute bleeding!uterus


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Etiology

Fetal factors!cardiovescular dysfunction

!deformity umbilical cord and placental factors

!abnormal cord:entanglement"

nuchal umbilical cord

prolapse of cord

!abnormal placenta


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Causes of Hypoxia*

risk factors

Maternal ris# factors

$iabetes

%regnancy-induced or chronic hypertension

Maternal infection

&ic#le cell anemia

'hronic substance abuse

(sthma &ei)ure disorders

%ost-term or multiple-gestation pregnancy


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Intrapartum causes of fetal

hypoxia**

(bnormal presentation of the fetus *i.e.

breech+

%remature onset of labor ,upture of membrane more than hours

prior to delivery

%rolonged labor

(dministration of narcotics and anesthetics


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Maternal hypoventilation Maternal hypoxia

Hypotension can be caused by either

epidural anaesthesia or the supine position"hich reduces inferior vena cava return ofblood to the heart. /he decreased bloodflo in hypotension can be a cause of fetal

distress *supine hypotension syndrome00+.


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Pathophysiology

Hypoxia1!(cidosis----sympathetic nerve excited----

hypertension"

tachycardia *initial signs+

!profound acidosis-----vagus nerve----

hypotension"

bradycardia"

hyperperistalsis----meconium discharge

!chronic condition: nutritional deficiency----F2,


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Clinical manifestation

'hronic fetal distress

!F2,

!dysfunction of maternal-placental-fetal unit!fetal heart monitoring

!fetal movement calculation

!amnioscopy


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Clinical manifestation

(cute fetal distress

!fetal heart rate

!characteristics of fluid!fetal movement

!acidosis


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How to define the newborn

asphyxia

3sually ith fetal distress.

(pgar score: 4-56 normal

-7 mild asphyxia

6- severe asphyxia


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Effects of Asphyxia

Fetal hypoxia is associated ith severecomplications in all systems. /he infant maysuffer:

Hypoxic ischemic encephalopathy

Meconium aspiration syndrome

(cidosis ith decompensation

'erebral palsy

8eonatal sei)ures


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ecunium

8ormal condition: mature of colon

Fetal hypoxia can stimulate fetal coloniccontraction that leads to evacuation of meconium

*fetal stool+ into the amniotic fluid

Ho meconium is dealt ith ill depend on hatit loo#s li#e and hat your provider9s approach is.

ld meconium is yello and less li#ely to be aproblem .


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econium

/hic#" green" particulate meconium hich may havealready caused baby to ;gasp; in utero.

If the meconium is accompanied by decreased heart ratesthat do not recover ell" a c-section ill be the safestapproach.

Fetal gasping due to the lac# of oxygen hich then causesaspiration of the meconium into the lungs.

/he presence of this material can produce bronchialobstruction and a chemical pneumonitisand treatment must

be initiated during delivery. If not ade


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econium aspiration most often

occurs in

/erm infants

2roth-retarded infants

%ost-term infants =reech presentation delivery

/he degree of meconium aspiration and the length ofexposure to meconium determines the severity of the

hypoxia suffered by the fetus. &taining of the umbilicalcord" s#in" or nails of the infant indicates exposure tomeconium to > hours in utero prior to delivery.


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Assessment

**

Antepartum Testing:

/ests for antepartum fetal evaluation include:

Fetal movement count

8on stress test

'ontraction stress test

=iophysical profile


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Fetal mo!ement

Fetal movement counts are performed by the

mother and are an inexpensive" noninvasive

method of assessing fetal ell-being. /he patient

records the number of times she feels fetal

movement ithin a designated time period. /he

exact number of normal perceived movements has

not been determined" hoever approximately 56movements should be felt ithin a 5 hour period.


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"on #tress $est %"#$&

/he is an indirect measurement ofuteroplacental function andre


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Contraction #tress $est %C#$&

'&/ or oxytocin challenge test" is more

costly and presents more of a ris# to the

fetus. but identifies fetal reserve duringcontractions. /he test measures late

decelerations during contractions induced

by either nipple stimulation or oxytocin

infusion. /he test is negative if no late

decelerations are observed.


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'iophysical profile

fetal movement

amniotic fluid volume

respiratory movement

movement of extremity

8&/


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Intrapartum Testing

/ests utili)ed to assess fetal ell being during

labor include:

Intermittent auscultation of the fetal heartrate

'ontinuous electronic fetal monitoring

&calp pH measurement


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Measurement of the fetal heart rate: abnormaldecelerations and decreased variability duringcontractions are suggestive of fetal distress.

Intermittent auscultation of the fetal heart rate is areliable indicator of fetal ell being and can beused in lo ris# deliveries. ,outine electronicfetal monitoring is not recommended for lo-ris#

omen in labor hen ade


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'ontinuous intrapartum fetal monitoring is

the mainstay in most modern obstetric units.

/he heart rate of the fetus is monitored todetect increases or decreases during

contractions. /he variability and trends are

interpreted to determine fetal distress or

ell being.


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&calp pH measurement helps to determinethe presence of acidosis and fetal hypoxiaand may influence the decision of

hether to continue observation or toperform a cesarean delivery. 8eurologicdeficits usually occur hen there is asevere acidosis" due to hypoxia" present at

birth. &evere hypoxia ill often causehypoxic-ischemic encephalopathy in theinfant.


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(hat)s the typical signs of fetal

distress**

/ypical signs of fetal distress include :

late heart rate decelerations

variable decelerations

prolonged bradycardia

indications of meconium staining.


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Intrapartum hypoxia is thought to be the

leading cause of cerebral palsy and no

accounts for to 5?@ of cerebral palsycases. 'hronic fetal hypoxia" caused by

maternal smo#ing or anemia" may also

contribute to a predisposition for &udden

Infant $eath &yndrome *&I$&+.


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Treatment of Hypoxia

MotherAs condition must be treated to prevent

hypoxia to the fetus including:

=lood pressure stabili)ation

Maternal positioning on the left side

Monitoring maternal oxygenation %elvic exam to identify cord presentation


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Treatment of Hypoxia

xygen administration to the mother may provideadditional availability of oxygen to the fetus.

/rained neonatal resuscitation staff should be

available at all times and should be present in the

delivery suite for those patients ith #non ris#for fetal distress or hypoxia.

'esarean sections are performed if all else fails"

and are the last alternative hen faced ith the

possibility of fetal distress.


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The decision to delivery interval

Medical litigation is on the rise in ourcountry particularly ith relation toobstetrics. /he day is not far henpremiums for malpractice nsurance riseparallel to the rise in the compensationoffered for these cases. MaBority of the

cases seem to be due to the delay in thedecision to delivery interval rather than theproblems ith diagnosis.


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(lthough there is poor correlation beteen FH,patterns and long term outcome a significantassociation has been noted beteen the decision to

delivery interval and admission to the neonatalintensive care unit for neonatal asphyxia

(n effort must be made to reduce the decision todelivery interval and restrict it to not more than 6minutes. It should be the norm to #eep the omen

and her relatives apprised of the situation of thelabor at all times and involve them in the decisionma#ing.


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In some cases of fetal distress immediate operativedelivery may be the only option to ensure ahealthy neonate. Cven in these situations

intrauterine resuscitation can play a role inenhancing the perinatal outcome. 3ltimately"efficient management and a good outcome in casesof fetal distress reflects a strong infrastructure and

good coordination beteen the obstetrician" thenursing staff" the staff in the operation room andthe neonatologist.


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Premature rupture of membrane%P+,&


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(hat is premature rupture of

membranes**

/he diagnosis of %,M is made henever the bag

of ater ruptures before the onset of true labor.

%%,M: %reterm premature rupture of

membranes is the rupture of membranes during

pregnancy before 7 ee#s9 gestation.

It occurs in percent of pregnancies and is the

cause of approximately one third of pretermdeliveries.


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Incidence

Daried greatly .7@--57@

%,M is causally related to about 56@

perinatal deathsregardless of gestation age.Its occurrence before term adds the ris# of

neonatal respiratory distress syndrome

*8,$&+ from hyaline membrane disease tothe ris# of chorioamnionitis " neonatal

sepsisassociated ith ascending infection.


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What causes premature rupture of

membranes?** /he exact etiology of %,M remains

un#non" there have been many postulated

causes" but a single common denominator

has not yet been found.


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membranes?**

Infection: subclinical infection" chorioamnionitis

coitus : patients ho had coitus ithin 7 days before delivery.

lo socioeconomic conditions : less li#ely to receive properprenatal care+

sexually transmitted infections such as chlamydia andgonorrhea

h f


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membranes?**

%revious preterm birth

Daginal bleeding

'igarette smo#ing during pregnancy

/rauma

'ervical incompetenceEcervical lacerationsEcervical operations

%olyhydramniosEmultiple gestations =lac# patients are at increased ris# of preterm

%,M compared ith hite patients.


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membranes?** un#non causes

/here appears to be no single etiology of

preterm %,M. It is li#ely that multiplefactors predispose certain patients to

preterm %,M.


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Complications of reterm !"#

Complications Incidence (%)

Delivery within one week 5 to !5

"espiratory distress syndrome #5

Cord compression #$ to !

Chorioamnionitis to

A'ruptio placentae to &$

Antepartum etal death & to $


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What are the symptoms of !"#?

/he folloing are the most common

symptoms of %,M. Hoever" each

oman may experience symptomsdifferently. &ymptoms may include:

lea#ing or a gush of atery fluid from the

vagina constant etness in panties

H i f


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Ho$ is premature rupture of

membranes diagnosed?*

In addition to a complete medical history and physical examination"%,M may be diagnosed in several ays" including the folloing:

an examination of the cervix *may sho fluid lea#ing from the cervicalopening+

testing of the pH *acid or al#aline+ of the fluid accuracy rate:->@

False-positive:

cervicitisEvaginitisEpresence of semen "al#aline urineEblood invagina

loo#ing at the dried fluid under a microscope *may sho a characteristicfern-li#e pattern+


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anagement

Hospitali)ation

expectant management *in some cases of

%%,M" the membranes may seal over and

the fluid may stop lea#ing ithout treatment+

monitoring for signs of infection such as fever"

pain" increased fetal heart rate" andEor

laboratory tests


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anagement

corticosteroids that may help mature the lungs of thefetus *lung immaturity is a maBor problem of prematurebabies+. Hoever" corticosteroids may mas# an infectionin the uterus.

antibiotics *to prevent or treat infections+

tocolytics - medications used to stop preterm labor.

delivery *if %,M endangers the ell-being of the

mother or fetus" then an early delivery may be necessaryto prevent further complications+


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Fetal Distress 3

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